Montserrat Roig, 2, 25008, Lleida, Spain. [email protected]

Aim: 

The consumption of polyphenols-rich foods has been extensively associated with the protection against the onset of several chronic diseases. Although, despite their high antioxidant capacity measured in vitro, and the reported biological effects, only micromolar concentration of dietary polyphenols in plasma have been reported. In previous results from our group, the polyphenols supplementation decreased most biomarkers of oxidative stress in several tissues and plasma risks factors of metabolic syndrome (cholesterol, triacylglycerols, insulin, glucose) without a significant change in plasma antioxidant capacity due to an unclear reason. Based on these observations, we hypothesize that some of these results may be related to modifications in the energy uptake or utilization. Therefore, we determine the effects of the supplementation of a polyphenols-rich beverage in energy utilization and mitochondrial profile in several mice tissues.

Methods: 

Two groups of mice (experimental & control) were randomly divided and fed a normal rodent diet. Experimental mice were supplemented for three months with a polyphenols-rich beverage and western blot analysis of tissue oxidative stress biomarkers (DNP, MDA-Lys, Neuroketals), mitochondrial content, complex I & III, AIF and AMPKa were performed in muscle, adipose tissue, liver, brain and heart.

Results: 

The amount of oxidative stress biomarkers was reduced considerably in most tissues (adipose tissue principally). In addition, higher levels of AMPKa were observed in the experimental group, which may have induced a higher mitochondrial content (for e.g. in muscle) of around 230%. The amount of complex I and III was also increased, without modifications in AIF content between groups.

Conclusion: 

Our results suggest that polyphenols supplementation may induce mitochondrial biogenesis (via AMPKa activation due a reduction in energy availability) which is related with a more efficient energy production that may contribute to reduce free radical production by the mitochondria and therefore to less tissue oxidative damage.